Alcohol abuse is one of the major health-related problems in the United States today. Clinical evidence links chronic alcohol intake to myocardial disease. The reversibility of this process is unknown. In addition, the cardiovascular effects of acute alcohol ingestion are not well defined. This is especially true in young adults and subjects without known heart disease. Alcohol induces comlpex changes in cardiovascular physiology. It reduces systemic vascular resistance while having variable effects on left ventricular (LV) shortening. Since there is an inverse relationship between afterload and the extent of LV shortening, alcohol would be expected to augment LV performance. However, prior studies using ejection fraction, shortening fraction, systolic time intervals, or cardiac output have shown slight improvement, no change, or even mild depression of LV function with acute alcohol ingestion. The utility of these traditional indices are limited by their inability to separate changes in LV performance from the effects of alterations in ventricular preload and afterload conditions. Our hypothesis is that the cardiotoxic effects of acute alcohol ingestion have been underestimated due to "masking" by the simultaneously occurring afterload reducing effects of the drug. Recently, indices of lV systolic performance have been defined in terms of physiologic events occurring at end-systole. These indices, which are sensitive to LV contractile state and independent of loading conditions will be determined noninvasively using echocardiographic and calibrated carotid pulse tracings in an attempt to define more fully the adverse cardiovascular effects of alcohol ingestion in humans. The specific aims to be addressed are: (1) Is there a difference in the LV contractile response to acute alcohol ingestion in alcoholic and non-alcoholic subjects without known heart disease? (2) Is there an age or sex related difference in the sensitivity to the myocardial effects of alcohol? (3) Is LV contractility in alcoholic and non-alcoholic subjects with mild-to-moderate congestive cardiomyopathy adversely and equally altered by acute ingestion of alcohol? and (4) Is there any improvement in LV contractility and contractile reserve capacity in chronic alcoholics who abstain from alcohol ingestion?